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Wednesday, October 29, 2014

Does this
sound like an oxymoron to you? It did to me, until I looked up the definition
of “bariatric.” According to Merriam-Webster online, it means “relating to or
specializing in the treatment of obesity.” And non-surgical bariatric medicine
is what Yoni Freedhoff, MD, an Ottawa, Canada-based family doc and Assistant
Professor at the University of Ottawa, practices.He is also the founder of Ottawa’s non-surgical
Bariatric Medical Institute, “a multidisciplinary, ethical, evidence-based
nutrition and weight management centre,” according to his Blogger website, www.weightymatters.ca. He quips
in his “About Me” that, “Nowadays I’m more likely to stop drugs than start
them.” He sounds like my kinda doc.

What
brought Dr. Freedhoff (I’m gonna call him Yoni) to my attention, I think, was
an email from my editor. “Sugar” has been one of her long-time “faves.” So,
when Yoni heralded Canada’s Heart and Stroke Foundation’s (HSF) issuance of
what he calls a “world leading sugar statement,” she gave me a heads up with this
link. And within Yoni’s post, he provides this
link to the HSF new position statement, “Sugar, Heart Disease and
Stroke.”

Yoni
describes the HSF position statement “as hard hitting as any I’ve read….” It
provides “a slew of recommendations” for consumers, the Federal and Provincial
Governments, and other regulatory bodies such as school boards. Some of the
recommendations, such as taxing sugar sweetened beverages and “Bloomberg style”
drinking cup size bans, I do not favor. Likewise they would have little chance
of enactment in the more individualistic, civil-libertarian political
environment of the U.S., but that’s not Yoni’s main thrust. It was what enabled the HSF to make their
recommendations possible in the first place. It was the HSF’s decision to “divorce themselves from their throngs of food
industry partners.”

Yoni’s dual
exhilaration is clear. He begins, “Huge kudos for Canada’s Heart and Stroke
Foundation,” and then he adds,

“Whether or not you agree with the HSF’s
recommendations, one thing’s incredibly clear, the HSF is no longer the food
industry’s partner – and that news is tremendous for Canadians as it’s amazing
how forceful and broad-sweeping public health organizations’ recommendations
can be when there’s no worry about upsetting industry partners.”

Yoni goes
on, “While reading this position piece and in it the HSF’s clear
unadulterated-by-industry voice, I couldn’t help but wonder what sort of forces
Dietitians of Canada and the American Academy of Nutrition and Dietetics
[formerly the American Dietetic Association] could be were they to divorce
themselves from the throngs of food industry partners, for as it stands now,
they’re both rather toothless and certainly not describable as drivers of change
or true champions of health.” Boy, the Ottawa community is lucky to have this
kind of doctor serving the “non-surgical bariatric” population.

Muckraking
is a messy business, though. Many a good researcher, and practitioner as well,
has had their career ruined by going against the flow, unable to get research
funds or publication in a peer-reviewed journal, by trying to advance an
alternative hypothesis or clinical approach to practicing medicine. That hasn’t
deterred, among others, one of my favorite bloggers, Kris Gunnars, a medical
student who blogs regularly at Authority
Nutrition, an evidenced-based approach. His posts are always backed up
with citations in the medical literature, and he’s got a big following.

Kris
usually blogs about healthy eating, but occasionally he goes off on a tangent
into the politics of nutrition. One of my favorites was http://authoritynutrition.com/big-food-is-much-worse-than-big-tobacco/ in which
he takes off on the same American Academy of Nutrition and Dietetics, the
“professional” organization that is “the ‘biggest
organization of nutrition professionals in the world’ – they are the ones in
charge of licensing Registered Dietitians in the U.S.,” he says. Take a look at
that link and open the links he provides to see what a mess – what a disgrace,
really – our situation is.

Another
post of Authority Nutrition ishttp://authoritynutrition.com/15-million-reasons-for-low-fat-diets/. This one
takes off on the American Diabetes Association (ADA), which still recommends
that “people eat a low-fat, high-carb diet.
According to them, diabetics should eat 45-65 grams of carbohydrates per meal.” Kris calls that a “crime against humanity.”

Saturday, October 25, 2014

“As part of
a series in the British Medical Journal
on overdiagnosis, which looked at the risks and harms to patients of expanding
disease definitions, Yudkin and Montori analyzed the concept of prediabetes,” began
a Medscape Medical News article. The lead
author of the BMJ essay is John S.
Yudkin, emeritus professor of medicine, University College, London.

This is NOT
the
legendary John Yudkin, founding professor of the department of nutrition at
Queen Elizabeth College, London, who advocated for a low-carb dietary and
lobbied against sugar in the 60’s and 70s. That John Yudkin retired in 1971,
published “Pure, White and Deadly” in 1972, was promptly ostracized by
academicians and ridiculed like Atkins in the U.S., and died in 1995. Neither
is this John S. Yudkin a son of the famed MD; he’s probably a nephew though.

The arguments
the BMJ piece read like the “con”
side of an Oxford debate. The Medscape
author concludes, “The existential question of whether prediabetes is a useful
concept or should be abandoned is largely philosophical.” In this I agree, but
the arguments presented by Yudkin and Montori do raise several issues that
deserve consideration.

The first
is that “prediabetes is a heterogeneous concept,” e.g., definitions “overlap”
and from the start create confusion. The original concept of “intermediate
hyperglycemia,” Medscape points out,
was termed “impaired glucose tolerance” and was “based on the oral glucose
tolerance test (OGTT).” While used today and still the “gold standard,” this
procedure is time consuming and expensive. An endocrinologist I saw back in the
80’s had me tested in a hospital outpatient setting.

Then, in
1997 that procedure was supplanted by simply drawing blood and sending it to
the lab like other blood tests. This new “intermediate hyperglycemia” procedure
was called “Impaired Fasting Glucose” and was revised in 2003 “to expand the
range of qualifying values.” That was when the diagnosis of diabetes was
dropped from 140 to 126mg/dL and the new category of “prediabetes” created,
defined as two consecutive fasting glucose readings between 100 and 125mg/dL.

“Only
recently,” in 2010, Medscape
continues, “a nameless intermediate category based on A1c was designated.” It
is “nameless,” I suspect, to allow for the dust to settle. Since 2010 the
medical profession, through disciplinary rivalries, has engaged in internecine
battles on guidance to clinicians treating a likewise “heterogeneous” patient
population, allowing clinicians to treat some elderly or intractable patients
to an A1c of 8.0%.Prior to 1997 the ADA
defined DM as an A1c ≥7.0% (est.Aver.Glucose:154mg/dl), then in 2003 ≥6.5%
(eAG:140mg/dL), then, if we are to believe this chart, in 2010,
≥6.0% (eAG:125mg/dL). The ADA, however, as well as the WHO/IDF, now still
define DM as an A1c of ≥6.5% and A1c’s of 6.0% - 6.4% as “intermediate
hyperglycemia” and thus “prediabetes.” N.B: Others define full-blown DM as low
as 5.8%.

The second
issue that should be recognized in “the case against considering elevated but subdiagnostic levels of glycemia a
disease unto itself that deserves intervention” is whether such a diagnosis
“can provide benefit by precisely identifying those who will develop diabetes…”
That was a key question examined by the authors, Medscape says, and the surprising answer, Yudkin and Montori say,
regardless of how pre-diabetes is defined, is “no.” “Less than one half of all
such people develop diabetes within 10 years.” I knew it was less than 100%,
but “Less than one half…” came as a surprise to me.

“Another
important question is whether treatment for prediabetes can prevent diabetes
onset,” Medscape says. The answer to this important question, both Medscape and the BMJ authors say, is “yes,” the “diabetes risk among high-risk
individuals can indeed be reduced.” Whew!!! I haven’t been wasting my time for
the last several years. But here Yudkin and Montori take the position that
“diabetes onset was merely delayed by 2-4 years, at high cost and only among a
subset of the intervention groups.” This last sentence – especially the last
clause (“only among a subset of the intervention groups”), is critically
important for my readers. YOU want to
be a part of that subset that not only delays the onset of diabetes but reversesprediabetes. This exclusive club is a subset-of-the-subset
exception, and YOU can be a member,
really. But you have to change your diet.
Stop eating the carbohydrate foods (sugars and
starches) that raise your blood sugar. You have to recognize that your “sugar”
(glucose) metabolism is broken. If you’re “prediabetic,” you are carbohydrate intolerant.

Afterword: The best
part of this hyperbolic debate over the “risks and harms” of overtreatment were
the “comments” in the BMJ. Click on this link if you’re
interested. The first two are academic essays in themselves and, while good, got
just one or two “likes.” The 9th down was from a practicing doctor who argued
the “pro” prediabetes case. His short comment got 50 “likes” at last count
(including mine). I hope the editors and readers of the BMJ take note. And
besides, even if you never become diabetic, your heart disease and dementia
risk closely correlate with your blood glucose levels. Control your blood sugar!

Wednesday, October 22, 2014

Virtually
everyone who has blood taken at the doctor’s office these days gets a standard
“lipid panel.” The cholesterol test. Your doctor gets assayed values for Total
Cholesterol (TC) and High-density lipoproteins (HDL), the so-called “good”
cholesterol, and more recently a value for non-HDL cholesterol in lieu of very low density lipoproteins. It also
has a related measurement, serum triglycerides, a fat molecule circulating in
your blood. In addition to these measurements, the lipid panel also reports on
low density lipoproteins (LDL), a calculated
value using the Friedewald formula (LDL=TC-HDL-TG/5).

Your doctor
will use the Total Cholesterol, if it’s over 200mg/dL, to try to persuade you
to take a statin drug. Statins effectively lower LDL cholesterol, known as the
“bad” cholesterol, and therefore lower TC. (TC=HDL+LDL+TG/5). This is a dubious
benefit for virtually everyone except those with coronary artery disease
(CAD). In patients with existing coronary artery disease, statins are indicated
for secondary prevention, to prevent
a heart attack.

Most lipid
panels also include a ratio, Total Cholesterol to triglycerides (TC/TG), as a
cardiovascular “risk indicator.” Doctors use this to evaluate the risk of
cardiovascular events such as heart attack (Myocardial Infarction or MI),
stroke, and death, among other outcomes. In The Nutrition Debate #27, I
presented the case that “the
strongest predictor of a heart attack” is the ratio of triglycerides to
HDL cholesterol, or TG/HDL. That column, written three years ago, applies to
the general “healthy” population and has proved to be one of the most popular I
have written. It’s also one of my editor’s favorites.

A more recent study, published
in Clinical research in cardiology: official journal of the German Cardiac
Society, provides a fresh look at “Risk prediction with triglycerides in
patients with stable coronary disease on statin treatment.” The aim of this
prospective study was “to analyze the role of fasting and postprandial
triglycerides (TG) as risk modifiers in patients with coronary artery disease
(CAD).” The trial used standardized measurements of oral triglyceride and
glucose tolerance in 514 patients with stable CAD, confirmed by angiography,
95% of whom were treated with a statin.

After 48
months follow-up, using both fasting and postprandial measurements and primary
outcomes of cardiovascular death and hospitalizations, the researchers sought
to determine if either fasting and/or postprandial serum triglycerides were a
risk indicator and could predict the primary outcome. The results were
surprising – indeed, startling, in my opinion.

The RESULTS
were unequivocal. For fasting TG >150 vs. <106 mg/dL, the hazard ratio
(HR) was 1.79. Translation: If you have CAD and are taking a statin, and your
triglycerides are over 150 mg/dL, you have an ~80% greater chance of dying or
being hospitalized for CAD over 4 years than if your triglycerides are
<106/mg/dL.

The analysis
then concluded, “Risk prediction by TG was independent of traditional risk
factors, medication, glucose metabolism, [and] LDL- and HDL-cholesterol. Total
cholesterol [and] LDL- and HDL-cholesterol concentrations were not associated
with the primary outcome [cardiovascular death and hospitalizations].”

MY
TAKEAWAY: If you have been diagnosed with coronary artery disease (CAD), your
doctor will surely prescribe a statin, the guideline-recommended medication,
and you should take it. But remember
that your fasting serum triglycerides are an independent risk factor. Fortunately, they are also a modifiable
risk factor, which is to say, one that
YOU can change. But there’s no magic bullet. Prescriptions for
Niacin and fibrates work for some people, and may be indicated for very high
TGs, but the best way to lower your fasting serum triglycerides and to keep
them lowis with Omega 3 fatty acids (2g
fish oil/day) (http://www.nlm.nih.gov/medlineplus/druginfo/natural/993.html) and
lowering the carbs in your diet.

Your doctor
is not likely to have seen this research from the German Cardiac Society. My
intrepid editor found it for me.Besides, fasting serum triglycerides from 150- 199 mg/dL are currently
regarded as “borderline” in the medical guidelines, so your doctor will likely
says something inane like, “We’ll have to watch that,” or “Cut back on your
drinking.” But remember, the hazard ratio for “primary outcomes” for TGs above
150 mg/dL was 1.79. Do you want to become a statistic?

Take a look at The
Nutrition Debate #68, “Triglycerides,
Fish Oil and Sardines,” to see my n=1 odyssey with triglycerides. I started
out “borderline,” but my most recent TGs have been 51, 55, 34, 49, 47, 58, 54,
56, 65, 53, 31, 38, 52, 49, 50 and 34.

Saturday, October 18, 2014

In this video interview
with transcript from the recent European Association for the Study of
Diabetes (EASD) meeting, Anne Peters, MD, at medscape.com, interviews Saudi MD
and diabetologist Aus Alzaid. Dr. Peters asks, “…knowing the epidemic of
diabetes that you are having in Saudi Arabia, can you tell us what diabetes
care is like there?” Dr. Alzaid replies, citing International Diabetes
Federation figures, that “Saudi Arabia has the highest rate of diabetes in the
world after the small island nations in the Pacific.” Citing previous studies, he
says, 1 in 4 people after the age of 30 has diabetes.”

But that it seems is part and parcel of the
problem, Dr. Alzaid avers: “That part of the Middle East is steeped in history
and tradition and culture, which means a lot to people. Then we have diabetes
as a condition, which has to do with the person’s perception of the lifestyle
modifications that must be made.” “I don’t know of any Saudi family that
doesn’t have a member or two with diabetes,” he adds.

Dr. Peters replies by relating how she “work(s) with
the Latino population in East Los Angeles where everybody just shrugs and says,
‘Everyone in my family has diabetes, so of course I have it too.’” In this
respect I think the good doctors make a point. Resistance to change is strong,
and fatalism commonly prevails. But would that be so if there was a “treatment”
that worked? I read on in hope of enlightenment.

Dr. Peters: “Most healthy 30-year olds don’t go to
the doctor. Are you making a push to convince young, healthy people to be
checked earlier?”

Dr. Alzaid: “Absolutely, and there are messages
going out about lifestyle modification. In our institution, we have Diabetes
Awareness Day in November. [Whoopee!] It is still an overwhelming issue, and we
are doing research to find out why we have such a high rate of diabetes.”
[There’s money well spent…if it’s good
research. Read on and you decide.]

Dr. Peters:
“Have diet and rates of physical activity changed? What have you seen over the
course of your career?”

Dr. Alzaid: “Decades ago, people were more mobile.
Very little food was available in years gone by, but over recent decades, with
the dividends of good fortune [oil revenue], there has been a ‘constant feast.’

Okay, the
well-meaning Dr. Peters is turning the conversation to “diet and exercise,” the
Western meme that we are eating too much and exercising too little. Well, at
least the conversation is beginning to turn to diet. Let’s see where it goes.

Dr. Alzaid
continues: “There are cultural things that we adhere to as part of our social
etiquette. Food items such as rice and dates are very popular in our part of
the world, and they are obviously very heavy in terms of calories. Fizzy drinks
are commonly consumed.” That’s it, folks. That’s the good Saudi doctor’s
understanding of nutrition, as captured in this Diabetes-in-Control piece. It’s all about calories-in/calories-out.
True, there’s no mention of eating fat making you fat, or anything about
dietary cholesterol. But neither is there so much as a word about carbohydrates (think ‘rice’ and ‘dates’).

Newsflash,
Dr. Alzaid: Dates and rice and fizzy [sugary] drinks are all carbohydrates!
Sugar and starch! 100 grams of pitted dates, about 4 Medjool dates, are 277
calories, of which 266 (96%) are sugar, 7 protein and 1 fat, plus a little
indigestible fiber and ash. 100 grams of medium grain white rice, about 3.5
ounces, is 130 calories, of which 116 are carbohydrates, 10 protein and 2 fat.
I don’t know what kind of “fizzy drinks” Saudis use to quaff their thirst, but
I’ll assume (generously) it’s a Coca Cola. A 12 ounce (370g) cola is 152
calories, all sugar. That’s ten (10)
teaspoons of sugar in one can of “fizzy drink.”

So, I think
that Dr. Alzaid has identified the problem with the Saudi diet; he just hasn’t
named it correctly. The “constant feast” he refers to is a carbohydrate feast, not a
calorie feast. The fact that Dr.
Alzaid describes “rice and dates” (part of the Saudi social etiquette) as
“obviously very heavy in terms of calories” implies to me that it is his
understanding that it is the calorie content of these foods, not the
carbohydrate content, that is the cause of the Saudi diabetes epidemic. But
what is there to do about it? It’s a cultural thing, and “that part of the
Middle East is steeped in history and tradition and culture, which means a lot
to people.” To which Dr. Peters replies, empathetically, ‘Everyone…has
diabetes, so of course I have it too.’ Of course, it is a problem of education,
which both doctors point out emphatically.

And the Saudi
Ministry of Health has launched a public-awareness campaign “to tackle the
problem with the right lifestyle.” The right lifestyle? Diet and exercise? Eat
less (of the same carbohydrate-dominated diet) and move more? That is a
lifestyle change that is guaranteed to fail. Diabetics are carbohydrate
intolerant by definition. The best treatment for type 2 diabetes is a very low
carbohydrate diet. The ‘right lifestyle’ to prevent type 2 diabetes is a
reduced carbohydrate diet.

Wednesday, October 15, 2014

ThisDiabetes-in-Control news piece begins,
“Diabetes rates among adults in the United States are finally leveling off, new
data from the Centers for Disease Control and Prevention suggest.” The headline
of the piece is less speculative. It simply declares,
“Diabetes Rates in the US Have Finally Plateaued.” Headlines often do that.
They try to grab your attention. In this case, with the primary audience being
clinicians and other health care providers, it also has a self-congratulatory
tone that is entirely unwarranted, as the “fine print” of the article makes
clear.

The Diabetes-in-Control piece is based on “findings from a
National Health Interview Survey (NHIS) on both prevalence and incidence of
diabetes from 1980 to 2012” published online in the Journal of the American Medical Association (JAMA). Prevalence refers to its
widespread, existential presence
while incidence, in the
epidemiological sense, relates to the initial
appearance of a new condition (diabetes)
in the population. Both, in the NHIS survey, were self-reported by the patient.
The findings which led to the headline are a reduction of the incidence of type 2 diabetes in
the general population.

Among the
664,969 adults aged 20 to 79 who responded to the NHIS survey, the prevalence of diabetes was 3.5% in 1990,
7.9% in 2008, and 8.3% in 2012. The incidence
per 1000 people was 3.2 in 1990, 8.8 in 2008 and 7.1 in 2012. The annual
percentage change in both prevalence and incidence was not significant in the
1980s; however, both jumped significantly from 1990 to 2008. Then, from 2008 to
2012, prevalence plateaued and incidence diminished significantly.

“However,” Diabetes-in-Control highlighted, “both
diabetes incidence and prevalence continued to increase at a significantly
greater rate for young adults aged 20 to 44 years compared with older adults
and for black and Hispanic adults compared with white adults.” In addition,
“The rate of increase in prevalence was higher for those with a high school education
or less compared with those with more than a high school education.” Hmmm.
Another sociodemographic disparity. I wonder if dietary choices had anything to
do with that. (Catch the sarcasm, pullese.)

The
sub-head in the article asks, “Is It All About Obesity?” Phrasing it as a
question, of course, begs the answer. The author notes that a little
mumbo-jumbo (a statistical adjustment) “reduced the annual percent change in
incidence by about a third…” with the study author telling Diabetes-in-Control, “This suggests that the leveling off of
obesity that occurred over the same period explains a large part of the
diabetes plateau, but not all of it.” The knock-out punch was, “The BMIs in the
NHIS study were self-reported and therefore most likely underestimated.” Do ya
think? Do you even know your own BMI?

Searching
for another explanation for “the diabetes plateau” the Diabetes-in-Control author speculates, “Beyond obesity, other
possible influences on the reduction in diabetes rates include improvements in
diet and activity levels and changes in diagnostic criteria.” Wow! If I read
this correctly, the author implies that we are getting obese at a lower rate than before; that she adduces this from the
finding of this epidemiological study that since the incidence of diabetes
diminished significantly from 2008 to 2012, that obesity associated with the
incidence and prevalence of type 2 diabetes did as well.

The only
evidence she offers for this association – the decline in incidence of type 2
diabetes with an assumed decline in
obesity, contrary to all other studies of the population known to me – is
“improvements in diet and activity levels.” Oh, how I wish that it were so.
That we could realize an actual result by just saying it over and over: Improve
your diet and activity levels (eat a balanced, USDA recommended
one-size-fits-all diet and exercise more), and abracadabra you will become
thin.

Maybe the
explanation for “the diabetes plateau” lies instead in the “changes in the
diagnostic criteria.” Do you think this could affect the way that 664,969
people self-reported on their condition? Could that alone have “confounded” the
study results to the point that all the other “statistical adjustments” were
totally insignificant by comparison? Do ya think?

“The 1997 lowering of
the fasting plasma glucose cutoff from 140 mg/dL to 126 mg/dL may have
increased the diabetes incidence…,” the CDC study author noted. I love it! “May
have,” she says. Whereas, “… the more recent [2010] shift to use HbA1c for
diagnosis may have reduced it, since HbA1c detects fewer cases of
hyperglycemia,” she said. Interesting indeed, and contrary to my own
understanding. The reason the medical establishment has shifted from “fasting”
to A1c is for the express purpose of
capturing blood glucose postprandial “excursions,” i.e. hyperglycemic spikes
due to impaired glucose tolerance (IGT) over a 3-month period. Fasting glucose
testing does not do that. It just captures impaired fasting glucose.

Saturday, October 11, 2014

“400
Calorie Meals for Fall,” the email from fitday.com
proclaimed. Exciting, I thought. Small meals. I’m always looking for ideas for
small meals that are very low in carbs. The reason, besides the fact that I
have been a type 2 diabetic for 28 years, is that if they are very low carb, moderate protein and high fat, I
won’t be hungry after eating it. I will be able to eat just 3 small
meals a day, without snacks, and always feel satisfied. And I will
lose weight, which it seems we all always need to do.

So, I
opened it to find 10 more links to recipes that promised “delicious healthy
meals.” “Try any of these low-calorie dishes and see just how great it feels to
eat well while still staying healthy,” FITDAY urged. Sounds promising, I
thought, since FITDAY is well known for helping people who both need and want
to lose weight keep track of the macronutrients of the foods they eat.
Macronutrients are the carbohydrates, protein and dietary fats that add up
collectively to total calories. Carbs and protein each contain 4 calories per
gram, alcohol has 7, while fat contains 9 calories per gram.

So, I started reading the FITDAY descriptions
to check them out. And sure enough each of the 10 small meals was 400 calories
or less. I noticed, however, that only
the total calories and fat grams were provided in the FITDAY write-ups. There
was no mention of carbs or protein in the FITDAY narratives. Okay, I thought,
that’s “old thinking.” Most dieters still think that only calories count and
that dietary fat makes you fat. But, for the enlightened reader, a fuller
nutritional analysis is necessary and surely would be included with the
recipes. So, I looked further.

Each link
opened to a different website that provided the ingredients and preparation
needed to make each meal. Of the 10 links, however, only 5 provided a
nutritional analysis, usually as a sidebar. And of those, the carb counts per serving for these small meals were humongous, including 41g for recipe #4;
45g for #5; and 47g for #10. Those numbers were so large that 1) fat burning would be impossible (the body
will burn the carbs first), and 2) when the carbs were “burned,” the body
craves more carbs (the sugar burner’s “hunger syndrome”). If I ate these meals,
my blood sugar would spike like crazy
and then crash (leaving me both tired and hungry). Is this what FITDAY
means by “how great it feels” to eat “healthy meals”?

Okay, not
all FITDAY users are type 2 diabetics, or even pre-diabetics. But it’s safe to
infer that virtually all of them are overweight or obese, and overweight
correlates very highly with pre-diabetes and type 2 diabetes. In fact, it is
the leading “risk factor” for a diagnosis of type 2 diabetes. Somewhat over 85
percent of type 2 diabetics are overweight or obese, and the percent
of U.S adults (≥20 y.o.) who are overweight, including obesity, is 69
percent (2011-2012). So, why would FITDAY advocate that its users
“incorporate [these] delicious healthy meals into [their] daily diet”? That’s
worth pondering.

Well,
FITDAY could still believe that only
total calories and fat grams count. After all, the Dietary Dictocrats at the
USDA still tell us all (EVERYONE) to “eat less and exercise more.” But the
government will be the last bastion of misinformation in the cause of the
“diabesity” epidemic. And they will be preceded only by the AHA and the ADA,
whose corporate sponsorship by agri-business and big pharma are nearly as
corrupt and/or misguided as the Federal Government’s approach to funding
research. It’s just such a myopic view and dogmatic attitude towards obesity
research and public health policy that has plunged the entire U.S. population
into this 60-year dietary experiment, with the disastrous outcomes we see
unfolding before us.

Besides,
can we really blame FITDAY if their potential user population – those who are
exposed to their advertisers since their site is “free” – itself believes that
only total calories and fat grams count? That’s still the main message we hear
from main-stream media, both print and TV. After all, total “members” are how
FITDAY sells their site to advertisers. So, until the pendulum swings in favor
of using macronutrient distribution as the means to determine whether a meal is
“healthy,” we will continue to be blithely “misinformed” and not know that eating 400 calories meals that are low
carb, not low fat, will lead to 1) losing weight easily, 2) feeling satisfied
(full) longer, and 3) regulating blood sugar better with lower A1c’s.

But then,
if we all learned to do that, FITDAY would lose “members.” We would have
discovered 1) what foods cause us to gain weight (carbs, not dietary fat), 2)
feel hungry a few hours after eating, and 3) spike our blood sugars (if we have
impaired glucose tolerance). And that wouldn’t be good for (FITDAY’s) business,
specifically their advertising revenues.

Ask
yourself, when you have discovered “how great it feels” to eat “healthy meals”
that are low-carb, and you lose weight, and are full of energy, and your doctor
likes what he/she sees and pats you on the back, why would you need FITDAY?

Wednesday, October 8, 2014

Good news
from Sweden, via Vienna, the site of this year’s European Association for the
Study of Diabetes 2014 meeting. This
paper was presented by an epidemiologist from the Lund University
Diabetes Center in Malmö, Sweden. According to Medscape Medical News, who reported on it here, “people
who consume a large amount of high-fat dairy products… have a 23% lower risk of
developing type 2 diabetes than those who consume lower levels…” That’s good
news for full-fat yoghurt, cheese, cream and whole-fat milk fans. My Swedish
relatives, and people the world over, should be rejoicing.

Admittedly,
the portion size spread was large (>8 vs. <1), but that still accounted
for 20% of the 26,930 Swedish people aged 45 to 74 years included in the study.
Swedes do love their yoghurt with fruit and coffee and bread for breakfast.
What interested me most about this study, though, was that both the Swedish
scientists and the Medscape writer
reporting on it were both open to the findings. The Medscape banner was, “Big Intake of High-Fat Dairy May Be
Protective for Diabetes.” That has got to get the attention of skeptics, which
is to say, the mainstream medical establishment. That in itself is news.

Of course, I am probably being naïve. A large cohort
of the Swedish population is already eating LCHF (low-carb, high-fat). Andreas
Eenfeldt, MD,The
Diet Doctor, reported on that some time ago. And he was among the first
to herald the decision of the Swedish Government to change its official dietary
recommendations in this
post. So, the Swedish scientists who initiated this study,
declaring themselves to have “no relevant financial relationships,” were like
the camel who stuck his nose into the tent. Their aim was, “to clarify the risk
for type 2 diabetes associated with the intake of the main dietary [saturated]
fat sources – namely, meat, fish and dairy. I added “saturated” because PUFAs
(polyunsaturated fatty acids from vegetable and seed oils) have become the main
dietary fat source for most Americans (86% vs. 14%, according to this 2008
USDA report, “Dietary
Assessment of Major Trends in U.S. Food Consumption, 1970-2005,”page
12 and table 6).

In the
cloak of pure, unbiased science, to the extent that is possible, they accepted
certain tenets of “perceived wisdom” while opening the crack in the “growing
body of evidence supporting the need to shift the focus of dietary advice away
from nutrients like total or saturated fat to the differential healthfulness of
food sources like dairy products or meat.”The hazard ratios (HRs), after 14 years of follow-up, were striking.
Most impressive was that high-fat fermented milk [yoghurt] consumption …reduced
the risk of developing diabetes by 20%. The portion size here was just 180ml,
or 6oz (3/4 cup!).

As usual,
the scientists raised more questions than they answered, looking for new grant
money, obviously. One of them said, “To place the observed beneficial
association with high-fat dairy in context, it is important to tease out if the
higher risk of no association of low-fat dairy products with diabetes was
because low-fat products have extra added sugar instead, which
we know from other research to be detrimental” (emphasis added by me). She also
noted that, “Other beneficial health effects might be due to other beneficial
compounds in dairy, such as probiotics [present in fermented foods like cheese
and yoghurt] and other nonfat nutrients such as vitamins and minerals.”

Medscape also noted that while “previous
epidemiological studies have indicated a high intake of dairy products is
associated with a decreased risk of developing type 2 diabetes,” the Swedish
scientists said, ‘but it has been suggested that mainly low-fat dairy lies
behind the observations.’” However, Medscape
concludes, “The findings presented here suggest only high-fat content is
protective.” “In comparison with high-fat dairy products, a large
intake of low-fat dairy was associated with increased
risk for type 2 diabetes, but this association disappeared after additional
adjustment for protein.”

Another
interesting finding reported by Medscape
was that “molecules with odd numbers of carbon atoms (15 and 17), which are
found in dairy products such as yoghurt, cheese and milk, appeared to have a
protective effect. This contrasts with evidence suggesting that even-chain
saturated fatty acids, as found in alcohol and margarine [demonizing one by
association with the other] are associated with a greater risk for type 2
diabetes.” More studies (money) needed here too.

“The results in relation to intake of meat and meat
products were found to be in line with previous findings,” Medscape reported. “An increased risk for diabetes was found for
meat and meat products regardless of fat content.” The camel’s nose knows not to go any further. But Swedes
and Europeans in general love dairy and eat far less meat than Americans.

The Medscape
article doesn’t mention any finding with respect to the other source of dietary
saturated fat: fish. Fish is sacred to Scandinavians in general, and salmon is
29% palmitic acid, an even chained
saturated fat. The last time we visited Sweden, in every home we visited the
gracious host served salmon with a crème fraiche and caviar topping, with
aquavit and a beer chaser, of course. Yum, yum. And full-fat yoghurt and fruit
and coffee (no bread for me) for breakfast. Real food.

Saturday, October 4, 2014

When I was growing up, I remember
Doris Day singing “Que será, será.” I was 15 years old (in 1956), and I thought
of it as an optimistic song that held the promise of a future of boundless
opportunity and possibilities. Remember the lyrics?

When I was just a little girl

When I grew up and fell in love

Now I have Children of my own

I asked my mother

I asked my sweetheart

They ask their mother

What will I be

What lies ahead

What will I be

Will I be pretty

Will we have rainbows

Will I be handsome

Will I be rich

Day after day

Will I be rich

Here's what she said to me

Here's what my sweetheart said

I tell them tenderly

Que sera, sera

Que sera, sera

Que sera, sera

Whatever will be, will be

Whatever will be, will be

Whatever will be, will be

The future's not ours to see

The future's not ours to see

The future's not ours to see

Que sera, sera

Que sera, sera

Que sera, sera

What will be, will be

What will be, will be

What will be, will be

Que Sera, Sera

At the time it never occurred to me
that the actual message of the song, contained in the response, was
“fatalistic,” which it clearly was. It just never occurred to me. I think
that’s because I grew up in a privileged environment. I believed the answer to the question was, in large
part, up to me. As I grew older, I often thought about how chance played a role
in my destiny, but I still considered that I had free will and that I chose the
path in life that I travelled and the things that came of it.

The title of this blog post
challenges that premise. It is a simple declaration, from researchers at the
Centers for Disease Control and Prevention (CDC), that “approximately 40% of American
adults will develop diabetes in their lifetime.” And that, “In Hispanic men and
women, and non-Hispanic black women, the projected increased risk is even
higher, over 50%...” These findings came to my attention through a Diabetes-in-Control
news item reporting on a
paper in The Lancet.

The
Lancet’s hypothesis was that since diabetes incidence has increased
and mortality (in the total population) has decreased greatly in the USA, there
would therefore be “substantial changes in the lifetime risk of diabetes.” So
besides estimated “remaining lifetime diabetes risk,” the study also looked at
“life-years lost due to diabetes” and “years spent with and without diagnosed
diabetes.” “Because of the increasing diabetes prevalence, the average number
of years lost due to diabetes for the population as a whole increased by 46% in
men and 44% in women. Years spent with diabetes increased by 156% in men and 70%
in women,” The Lancet’s statistical
analysis concluded.

The Lancet’s
INTERPRETATION of the CDC’s report and their (The Lancet’s) FINDINGS:

“Continued
increases in the incidence of diagnosed diabetes combined with declining
mortality have led to an acceleration of lifetime risk and more years spent
with diabetes, but fewer years lost to the disease for the average individual
with diabetes. These findings mean that there will be a continued need for
health services and extensive costs to manage the disease, and emphasise
the need for effective interventions to reduce incidence” (emphasis
added).

The Lancet’s and the CDC’s projections are a
dispassionate analysis of statistical trends - exactly what a study like this
is supposed to do. And the call for “the need for effective interventions to
reduce incidence” of diabetes should be a clarion message to the medical
establishment. Instead, the message that I think the medical establishment gets
is “that there will be a continued need for health services…to manage the
disease.” In other words, job security for the medical establishment in
managing (i.e., treating) the increasing numbers of diabetics and the
progressive course of the disease.

Okay, I am cynical
and maybe a bit unfair. I don’t doubt that The
Lancet is sincere about “the need for effective interventions to reduce
incidence.” Can they be blamed for a myopic view of what such interventions
might be? To confining their perspective to pharmacological treatments? New
drugs? Surgery? After all, they can report on public health policy and
nutrition research, but the government only seems willing to support research
in line with predetermined dogma of “good” public health policy and nutrition.
What hope is there that the outcome will be other than, “Whatever will be, will
be.” Que será, será.

Wednesday, October 1, 2014

If you have been diagnosed a type 2 diabetic, your
doctor (YOU actually) have a choice of long-term treatment options: 1) insulin
injections, 2) oral antidiabetic medications, or 3) major dietary changes. I’ve
oversimplified it, but this is an overview so the unschooled reader can see the
“big picture.” Besides, I’m not without my own biases, as you’ll see.

To illustrate the insulin route, I cite a rather pedantic
article,
originally published in 2011 in Diabetes in Control, a source which bills
itself as “News and Information for Medical Professionals.” It was re-posted on
September 11, 2014, to promote the Humumin R insulin product. Why do I say
that? From the advertising. The article is accompanied by ads for Eli Lilly and
Company’s Humulin R,* as you scroll down the screen, 5 of them: top (1), side
(3) and bottom (1). In fact, a hyperlink under the title reads, “Humulin Insulin
Special Edition September 2014.” Maybe the whole article is just a paid
advertisement.* Specifically the U-500 version, a concentrated form for
insulin-resistant patients requiring more than 200 units a day.

I have nothing against injecting insulin. Insulin is
a good thing, and it works. And I have nothing against advertising. I do have a
problem, however, when advertising and clinical practice advice get mixed
together. I have an even bigger problem when the first two authors of the piece
just happen to be Editor-in-Chief and Publisher, respectively, of the Diabetes
in Control “newsletter.”I didn’t know
that, however, because it is revealed in the “disclosures,” as it is in a
peer-reviewed medical journal. There are no disclosures. I knew it because I
have been reading this “information source for medical professionals” for
years.

But if you
didn’t know, and care to go to the trouble, Google David Joffe (the Diabetes in Control
Editor-in-Chief), and learn, “Dave speaks on diabetes, hypertension, and
related co-morbidities for Abbott, Bayer, Pfizer,
Novo Nordisk, Lilly, Sanofi, Sankyo, and Medtronic” (emphasis added). Or, “Dave
is a non-physician member of the Lilly Primary Care Diabetes Advisory Board.”
Admittedly, conflicts aside, reading his full curriculum vitae, the guy has mega bona fides.

Nevertheless, the “Practice Pearls” for insulin as a
treatment for newly diagnosed Type 2s are a good “takeaway”:

●By removing the glucolipotoxicity you can improve beta cell function.

●Since Type 2 diabetes is a
progressive disease and will worsen over time, by improving beta cell function
the progression of diabetes can be slowed down to prevent complications

The 2nd long-term treatment option is also
pharmacotherapy. Oral antidiabetic medications have evolved from the early days
when insulin-secreting sulfonylureas were the only option. Today most newly
diagnosed type 2 diabetics and even “pre-diabetics” (those that can “tolerate”
it) are started on metformin. The dose is quickly increased (“titrated”) until
you are “maxed out” and then a second agent, and even a third med is added to
the “cocktail.” Since, as we’ve seen above (in the 2nd bullet), the
“perceived wisdom” is that “type 2 diabetes is a progressive disease and will
worsen over time,” the assumption is that many type 2 diabetics who are treated
with orals will “progress” to insulin dependency.

The major downside to injecting insulin is hypoglycemia,
or low blood sugar. It can lead to coma and death. That is because you, the
patient, has to decide on the amount to inject before each meal or snack.Your care giver can help on the amount of
“basal” insulin you inject once or twice a day, but only you can decide how
much to inject before each meal ‘cause your doctor is not at your side 24/7.
Even if you have a pump and continuous glucose monitoring (CGM), which few do, you have to figure the dose of mealtime
insulin that you inject each time. As
a result, many patients, and their caregivers including clinicians and CDEs, do
not try for “tight glucose control.” They inject too little to avoid the danger
of hypoglycemia.

The exception to this would be the pioneer on
glucose meters, glucose monitoring, and low-dose insulin regimens, Dr. Richard
K. Bernstein. His book, Diabetes Solution, is an authoritative source
for all diabetics. And Dr. Bernstein’s Diabetes Forum (registration required),
accessed from the same link, is a great place for learning about all aspects of
diabetes.

The downside for oral antidiabetic medications is 1)
all drugs have side effects and 2) if you do nothing else and just let your
doctor monitor and treat your worsening glucose metabolism, your type 2
diabetes will “progress” and “worsen
over time.” And if the progression of the disease cannot be slowed down, you
run the risk of developing “the dreaded
complications,”
not to mention macrovascular
complications like heart disease.

Now, the 3rd
long-term treatment option for type 2 diabetes or pre-diabetes: major dietary
changes. Pros: no insulin (and no hypos), few if any oral meds (and no side
effects from same), and greatly improved
(not worsening) glucose control, plus a bonus: improved BP and blood lipids
(higher HDL, lower triglycerides, stable Total Cholesterol and LDL). Less of
that nasty MG (see
The Nutrition Debate #246 here) stuff too. And another under recognized
benefit: you will lose weight, have lots of energy and feel great! Cons: you
have to give up the processed foods and carbohydrate-loaded junk that made you
sick in the first place. It’s your choice. And yours alone.

About Me

I was diagnosed a Type 2 diabetic in 1986. I started a Very Low Carb diet (Atkins Induction) in 2002 to lose weight. I didn’t realize at the time that it would put my diabetes in clinical remission, or that I would be able to give up almost all of my oral diabetes meds. I also didn’t understand that, as I lost weight and continued to eat Very Low Carb, my blood lipids would dramatically improve (doubling my HDL and cutting my triglycerides by 2/3rds) and that my blood pressure would drop from 130/90 to 110/70 on the same meds.
Over the years I changed from Atkins to the Bernstein Diet (designed for diabetics) and, altogether lost 170 pounds. I later regained some and then lost some. As long as I eat Very Low Carb, I am not hungry and I have lots of energy. And I no longer have any of the indications of Metabolic Syndrome.
My goal, as long as I have excess body fat, is to remain continuously in a ketogenic state, both for blood glucose regulation and continued weight loss. I expect that this regimen will continue to provide the benefits of reduced systemic inflammation, improved blood lipids and lower blood pressure as well.